Component
Cancer-cell clonogenic survival
Ability of cultured cancer cells to form colonies after experimental treatment.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Ferritin-heavy-chain overexpression in H1299 cells lowered labile iron and increased clonogenic survival after pharmacological ascorbate, supporting a protective role of intracellular iron sequestration in this setting.
Experimental context and source evidence
- cross_nutrient
- true
- evidence_location
- Figure 6I–L
- experimental_model
- H1299 adenoviral ferritin-heavy-chain versus empty-vector cultures; calcein/BIP and clonogenic assays
- exposure
- 20-MOI ferritin-heavy-chain expression 36 h before experiment; 5 pmol/cell (approximately 2–3 mM) ascorbate for 1 h.
- limitations
- Engineered overexpression is not dietary iron deficiency or ordinary ferritin concentration; serum ferritin does not measure this intracellular intervention.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Homo sapiens
- plain_language
- Locking more iron into ferritin protected these lung cancer cells from the exposure.
- primary_references
- [c-reg-schoenfeld] O2⋅- and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate. (2017). https://pubmed.ncbi.nlm.nih.gov/28366679/ DOI: 10.1016/j.ccell.2017.02.018
- tissue_or_cell_type
- NSCLC cells
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1369–1381
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · H1299 adenoviral ferritin-heavy-chain versus empty-vector cultures; calcein/BIP and clonogenic assays · source_derived_draft · unverified_draft
### c-reg-ferritin-heavy-protects Ferritin-heavy-chain overexpression in H1299 cells lowered labile iron and increased clonogenic survival after pharmacological ascorbate, supporting a protective role of intracellular iron sequestration in this setting. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Locking more iron into ferritin protected these lung cancer cells from the exposure. organism: Homo sapiens tissue_or_cell_type: NSCLC cells experimental_model: H1299 adenoviral ferritin-heavy-chain versus empty-vector cultures; calcein/BIP and clonogenic assays limitations: Engineered overexpression is not dietary iron deficiency or ordinary ferritin concentration; serum ferritin does not measure this intracellular intervention. exposure: 20-MOI ferritin-heavy-chain expression 36 h before experiment; 5 pmol/cell (approximately 2–3 mM) ascorbate for 1 h. cross_nutrient: true evidence_location: Figure 6I–L [c-reg-schoenfeld] O2⋅- and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate. (2017). https://pubmed.ncbi.nlm.nih.gov/28366679/ DOI: 10.1016/j.ccell.2017.02.018
Complete structured claim and evidenceSOD2 knockout A549 cells had higher basal labile iron and greater clonogenic killing by ascorbate than parental cells, linking antioxidant machinery impairment to sensitivity in this model.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Figure 5C–E
- experimental_model
- SOD2-null versus parental A549; calcein/BIP labile-iron assay and clonogenic survival
- exposure
- 10 pmol/cell (2 mM) ascorbate for 1 h; LIP measured with 500 nM calcein-AM and 100 µM 2,2′-bipyridyl dequenching.
- limitations
- SOD2 genotype is not dietary manganese deficiency; DHE oxidation alone is not chemically specific proof of superoxide. Study does not identify a universal cancer-selectivity mechanism.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Homo sapiens
- plain_language
- Removing a mitochondrial antioxidant enzyme made these lung cancer cells more vulnerable to the high-dose exposure.
- primary_references
- [c-reg-schoenfeld] O2⋅- and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate. (2017). https://pubmed.ncbi.nlm.nih.gov/28366679/ DOI: 10.1016/j.ccell.2017.02.018
- tissue_or_cell_type
- Lung adenocarcinoma cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1355–1367
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SOD2-null versus parental A549; calcein/BIP labile-iron assay and clonogenic survival · source_derived_draft · unverified_draft
### c-reg-sod2-loss-sensitizes SOD2 knockout A549 cells had higher basal labile iron and greater clonogenic killing by ascorbate than parental cells, linking antioxidant machinery impairment to sensitivity in this model. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing a mitochondrial antioxidant enzyme made these lung cancer cells more vulnerable to the high-dose exposure. organism: Homo sapiens tissue_or_cell_type: Lung adenocarcinoma cells experimental_model: SOD2-null versus parental A549; calcein/BIP labile-iron assay and clonogenic survival limitations: SOD2 genotype is not dietary manganese deficiency; DHE oxidation alone is not chemically specific proof of superoxide. Study does not identify a universal cancer-selectivity mechanism. exposure: 10 pmol/cell (2 mM) ascorbate for 1 h; LIP measured with 500 nM calcein-AM and 100 µM 2,2′-bipyridyl dequenching. cross_nutrient: true evidence_location: Figure 5C–E [c-reg-schoenfeld] O2⋅- and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate. (2017). https://pubmed.ncbi.nlm.nih.gov/28366679/ DOI: 10.1016/j.ccell.2017.02.018
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.